Neutrophils: release of mediators of inflammation with special reference to rheumatoid arthritis.
The encounter of neutrophils with immune complexes and complement components, in the bulk phase or on a surface, leads to their secretion of lysosomal hydrolases, especially neutral proteases, which provoke tissue injury. Secretion of lysosomal enzymes and generation of reactive oxygen species (e.g., O(2)) is part of a stimulus-secretion response to a variety of secretagogues, including immune complexes and complement components. However, the pathways of secretion and O(2) generation are stimulus-specific and can be dissected to establish cause and effect relationships by means of: a) kinetic analysis, b) variations in the stimulus, and c) use of impermeant reagents to block discrete responses. Neutrophils also generate products of 11-cyclooxygenase (e.g., PGE2, TxA2) and of the 5-and 15-lipoxygenases (mono-, di-, and tri-HETEs, LTB4, and their isomers). But the cyclooxygenase products (save TxA2) are not phlogistic by themselves: they inhibit the functions of neutrophils, platelets, macrophages, and mast cells. The most potent pro-inflammatory agent yet identified as a product of arachidonate is LTB4. LTB4 is a potent Ca ionophore, constricts airways, is a potent chemoattractant, and induces local inflammation.
D000818:Animals; D000936:Antigen-Antibody Complex / Q000378:metabolism; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000097:blood; D001172:Arthritis, Rheumatoid / Q000097:blood*; D006801:Humans; D007249:Inflammation / Q000097:blood*; D009504:Neutrophils / Q000378:metabolism*; D010084:Oxidation-Reduction
D000936:Antigen-Antibody Complex; D001095:Arachidonic Acids; D016718:Arachidonic Acid